Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes composed of multiple subunits, arranged to form ligand-gated ion channels. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. The subunit encoded by this gene belongs to a family of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate)-sensitive glutamate receptors, and is subject to RNA editing (AGA->GGA; R->G). Alternative splicing at this locus results in different isoforms, which may vary in their signal transduction properties. [provided by RefSeq, Jul 2008]
Forensic Context
A study in mice demonstrated that the GRIA3 is part of a common cosplicing network of glutamatergic synapse genes in brain reward circuitry regions, implicating glutamate-mediated synaptic plasticity in the risk for methamphetamine intake [Hitzemann et al. DOI:10.3390/brainsci9070155]. In human postmortem cerebellar tissue, the GRIA3 was analyzed via qRT-PCR as a candidate gene from a microarray study investigating hypoxia markers after traumatic frontal cortex injury, though its specific forensic discriminatory efficacy was not detailed among the final validated combinations [Schober et al. DOI:10.1007/s00414-014-1129-3]. A study in human post-mortem brain tissues demonstrated that the GRIA3 (GRIA3) mRNA was down-regulated in chronic traumatic encephalopathy (CTE), CTE with Alzheimer's disease (CTE/AD), and Alzheimer's disease (AD) compared to normal subjects, as identified through transcriptome sequencing and differential expression analysis [Cho et al. DOI:10.1038/s41598-020-65916-y]. This down-regulation was part of a broader finding where AMPA receptor subunits and other memory function-related genes were commonly decreased in these head trauma-related neurodegenerative disorders.